Emerging Effects of IL-33 on COVID-19.

Emerging Effects of IL-33 on COVID-19.
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DOI:
10.3390/ijms232113656
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发表时间:
2022-11-07
影响因子:
5.6
通讯作者:
--
中科院分区:
生物学2区
文献类型:
--
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自严重急性呼吸系统综合征冠状病毒2型(SARS-CoV-2)引起的COVID-19大流行开始以来,全球已有超过600万人直接或间接丧生。尽管人们加大了努力来阐明COVID-19的免疫病理学,但引发炎症风暴并导致患者严重临床结局的关键因素和过程仍不清楚。IL-33作为一种炎症风暴因子,是一种报警细胞因子,在细胞损伤或感染中起重要作用。最近的研究表明,血清IL-33在COVID-19患者中上调,并与不良结局密切相关。严重感染中IL-33水平的增加可能是由于激活的免疫细胞之间的强烈相互作用引起的炎症风暴。然而,IL-33在COVID-19中的作用及其潜在机制仍有待充分阐明。本文就IL-33在病理生理条件下的生物学特性及其对免疫细胞(包括中性粒细胞、先天性淋巴细胞(ILC)、树突状细胞、巨噬细胞、CD 4 + T细胞、Th 17/Treg细胞和CD 8 + T细胞)吞噬COVID-19的调节作用作一综述。本文旨在探讨IL-33/免疫细胞通路作为COVID-19早期诊断、重症病例监测和临床治疗新靶点的潜在价值。
Since the start of COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), more than 6 million people have lost their lives worldwide directly or indirectly. Despite intensified efforts to clarify the immunopathology of COVID-19, the key factors and processes that trigger an inflammatory storm and lead to severe clinical outcomes in patients remain unclear. As an inflammatory storm factor, IL-33 is an alarmin cytokine, which plays an important role in cell damage or infection. Recent studies have shown that serum IL-33 is upregulated in COVID-19 patients and is strongly associated with poor outcomes. Increased IL-33 levels in severe infections may result from an inflammatory storm caused by strong interactions between activated immune cells. However, the effects of IL-33 in COVID-19 and the underlying mechanisms remain to be fully elucidated. In this review, we systematically discuss the biological properties of IL-33 under pathophysiological conditions and its regulation of immune cells, including neutrophils, innate lymphocytes (ILCs), dendritic cells, macrophages, CD4+ T cells, Th17/Treg cells, and CD8+ T cells, in COVID-19 phagocytosis. The aim of this review is to explore the potential value of the IL-33/immune cell pathway as a new target for early diagnosis, monitoring of severe cases, and clinical treatment of COVID-19.
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